Molecular and cellular mechanisms of myocardial remodeling

被引：35

作者：

Maytin, M

Colucci, WS

机构：

[1] Boston Univ, Med Ctr, Dept Med, Cardiovasc Med Sect, Boston, MA 02118 USA

[2] Boston Univ, Sch Med, Myocardial Biol Unit, Boston, MA USA

来源：

JOURNAL OF NUCLEAR CARDIOLOGY | 2002年 / 9卷 / 03期

关键词：

D O I：

10.1067/mnc.2002.123207

中图分类号：

R5 [内科学];

学科分类号：

1002 ; 100201 ;

摘要：

Myocardial remodeling is inextricably intertwined with the development and progression of heart failure. It is characterized by alterations in ventricular geometry and function. At the cellular level, ventricular remodeling consists of myocyte hypertrophy, neurohumoral activation, matrix remodeling, altered gene expression, immune system activation, and apoptosis. Many factors, including neurohormones, cytokines, growth factors, oxidative stress, and mechanical strain, can trigger the molecular and cellular events observed in remodeling, thus suggesting that they may play a role in myocardial remodeling. A thorough understanding of the cellular and molecular mechanisms involved in myocardial remodeling may lead to novel pharmacologic or genetic therapies for the treatment and prevention of heart failure.

引用

收藏

页码：319 / 327

页数：9

相关论文

共 111 条

[91] Angiotensin II, adhesion, and cardiac fibrosis [J].

Schnee, JM ;

Hsueh, WA .

CARDIOVASCULAR RESEARCH, 2000, 46 (02) :264-268

[92] NOREPINEPHRINE-STIMULATED HYPERTROPHY OF CULTURED RAT MYOCARDIAL-CELLS IS AN ALPHA-1 ADRENERGIC RESPONSE [J].

SIMPSON, P .

JOURNAL OF CLINICAL INVESTIGATION, 1983, 72 (02) :732-738

[93] Inhibition of copper-zinc superoxide dismutase induces cell growth, hypertrophic phenotype, and apoptosis in neonatal rat cardiac myocytes in vitro [J].

Siwik, DA ;

Tzortzis, JD ;

Pimental, DR ;

Chang, DLF ;

Pagano, PJ ;

Singh, K ;

Sawyer, DB ;

Colucci, WS .

CIRCULATION RESEARCH, 1999, 85 (02) :147-153

[94] Interleukin-1β and tumor necrosis factor-α decrease collagen synthesis and increase matrix metalloproteinase activity in cardiac fibroblasts in vitro [J].

Siwik, DA ;

Chang, DLF ;

Colucci, WS .

CIRCULATION RESEARCH, 2000, 86 (12) :1259-1265

[95] Oxidative stress regulates collagen synthesis and matrix metalloproteinase activity in cardiac fibroblasts [J].

Siwik, DA ;

Pagano, PJ ;

Colucci, WS .

AMERICAN JOURNAL OF PHYSIOLOGY-CELL PHYSIOLOGY, 2001, 280 (01) :C53-C60

[96] A matrix metalloproteinase induction/activation system exists in the human left ventricular myocardium and is upregulated in heart failure [J].

Spinale, FG ;

Coker, ML ;

Heung, LJ ;

Bond, BR ;

Gunasinghe, HR ;

Etoh, T ;

Goldberg, AT ;

Zellner, JL ;

Crumbley, AJ .

CIRCULATION, 2000, 102 (16) :1944-1949

[97] Time-dependent changes in matrix metalloproteinase activity and expression during the progression of congestive heart failure - Relation to ventricular and myocyte function [J].

Spinale, FG ;

Coker, ML ;

Thomas, CV ;

Walker, JD ;

Mukherjee, R ;

Hebbar, L .

CIRCULATION RESEARCH, 1998, 82 (04) :482-495

[98] Matrix metalloproteinase inhibition during the development of congestive heart failure - Effects on left ventricular dimensions and function [J].

Spinale, FG ;

Coker, ML ;

Krombach, SR ;

Mukherjee, R ;

Hallak, H ;

Houck, WV ;

Clair, MJ ;

Kribbs, SB ;

Johnson, LL ;

Peterson, JT ;

Zile, MR .

CIRCULATION RESEARCH, 1999, 85 (04) :364-376

[99] HYPERTROPHIC STIMULI INDUCE TRANSFORMING GROWTH FACTOR-BETA(1) EXPRESSION IN RAT VENTRICULAR MYOCYTES [J].

TAKAHASHI, N ;

CALDERONE, A ;

IZZO, NJ ;

MAKI, TM ;

MARSH, JD ;

COLUCCI, WS .

JOURNAL OF CLINICAL INVESTIGATION, 1994, 94 (04) :1470-1476

[100] EXPRESSION OF A-TYPE, B-TYPE, AND C-TYPE NATRIURETIC PEPTIDE GENES IN FAILING AND DEVELOPING HUMAN VENTRICLES - CORRELATION WITH EXPRESSION OF THE CA2+-ATPASE GENE [J].

TAKAHASHI, T ;

ALLEN, PD ;

IZUMO, S .

CIRCULATION RESEARCH, 1992, 71 (01) :9-17

← 3 4 5 6 7 8 9 10 11 12 →